Additionally, there are more and more studies indicating that SAVs are also associated with several cancers (Lori et al., 2013; Niroula & Vihinen, 2015; Song et al., 2014). Cancer, which is caused by a particular change to chromosome, is often regarded as a genetic disease. However, the mechanism is distinct from Mendelian diseases, and little do we know this complicated network. Until now, a large number of studies reveal massive radical changes in cancer patient genomic sequences. Investigated mutation spots are often biomarkers or targets for treatment (Ma et al., 2018; Nie et al., 2014; Renaud et al., 2016). Previous studies reported that a set of missense variations that disrupt protein function was associated with cancer (B. Li et al., 2009). Recent studies suggested that the accumulation of somatic mutation is a vital factor in carcinogenic progress. Some variations seem neutral, but they might contribute to cancer progressing, known as driver mutation (McFarland et al., 2017). However, identifying the trigger point preciously is still not easy, but observing the accumulation of possibly threatening is very helpful. In the proteome level, amino acid substitution caused by genetic codon transition might be the reason for human cancer (Son, Kang, Kim, & Kim, 2017). The chemical properties of replaced amino acid could lose or gain protein function. Besides, amino acid alteration seems to follow special rules. For example, arginine has a positive charge that is important to balance the charges of protein and DNA binding; however, it is highly mutated in various cancer types. The loss of function of cancer-associated proteins is frequently due to the loss of arginine.